Antibody induced abortion in pp women affecting P1 but not P2 pregnancies has been associated with IgG anti-P1 specificity directed to P1 sites in the fetal rbc but also to P1 sites in fetal tissue cells. Exceptions have been noted in two independent studies and the explanation for P1 pregnancies escaping abortion and going to term is based on high numbers of fetal P1 sites remaining at end of the first trimester. Most frequently P1 sites are considerably diminished to a level where they induce an active immune response so that the excess of IgG anti-P1 molecules exert cytotoxicity on the greatly diminished P1 sites and hence abortion. When P1 sites remain at high levels at the end of the first trimester, these absorb anti-P1 which now is incapable of any cytotoxic effect on the excessive number of P1 sites. The stepwise addition of a sugar by action of specific transferase from pk yields P (globoside) yields Fs (Forssman) and p yields P1 is fundamental and relates to the presence of a precursor with antibodies in the serum for its next sugar in the normal mucosa and the next final product in the adjacent adenoca. This holds true for P yields Fs and p yields P1. Also when the transferase normally converting pk completely to P is absent, the very rare pkpk accumulates. This serves as an example of the one gene-one enzyme and is the genetic basis for the group of inborn errors of metabolism as defined by Garrod and established in the experimental model of Beadle and Tatum. It is also compatible with the self-nonself concept as defined by Levine.